中文摘要：

目的观察佐芬普利对大鼠肥大心肌细胞ACE2和Mas受体的影响。方法原代培养大鼠心肌细胞，随机分为3组：正常组、模型组、实验组。模型组与实验组以去甲肾上腺素干预，致细胞肥大；48h后，实验组加佐芬普利干预。RT—PCR法检测正常组、模型组的心肌细胞脑钠肽（BNP）mRNA水平及各组ACE2和MasmRNA表达水平，Westernblotting技术检测两者蛋白表达水平。结果去甲肾上腺素诱导48h后，体外培养的心肌细胞BNPmRNA水平较正常组显著升高（P〈0．01）；与正常组相比，模型组心肌细胞ACE2和MasmRNA及蛋白水平无明显变化（P〉0．05）。实验组较模型组ACE2显著升高（P〈0．01），Mas轻度升高（P〈0．05）。讨论去甲肾上腺素成功诱导心肌细胞肥大，佐芬普利逆转心肌肥厚作用，可能与其上调心肌细胞ACE2和Mas受体表达有关。

英文摘要：

Objective To study the effect of reversal the hypertrophic cardiomyocytes and ACE2/angiotensin （ 1 - 7 ）/Mas receptor axis in cel- lular level of zofenopril, which provides the theoretical basis with reversal of myocardial remodeling. Methods Cultivation of rat primary myocar- dial cells, intervened 48 hours by norepinephrine to make mast cells, then added with zofenopril to culture continue. Randomly divided into three groups with all cells：normal group, model group and experiment group. After 48 hours with norepinephrine, tested brain natriuretic pep- tide （BNP） mRNA between normal group and model group by RT- PCR. Detected mRNA levels of ACE2 and Mas of each group by RT - PCR, and tested the protein expressions of ACE2 and Mas receptor by western blotting. Results BNP mRNA level of myocardial cells signifi- cantly increased （P 〈 0. 01 ） after 48 hours with norepinephrine com- pared with normal group. Compared with normal group, ACE2 and Mas receptor mRNA and protein expression without obvious changes （P 〉 0. 05） in model group; compared with model group, ACE2 mRNA and protein expression were remarkable increased （ P 〈 0. 01 ） in experiment group, Mas mRNA and protein expression increased mildly （P 〈 0. 05 ）. Conclusion We can establish hypertrophic cardiomyocyte model suc- cessfully by norepinephrine. The zofenopril up- regulate ACE2 and Mas may have relationship with reversal of myocardial remodeling, provide new therapeutic targets for myocardial hypertrophy.